Tandon S K, Khandelwal S, Jain V K, Mathur N
Industrial Toxicology Research Centre, Lucknow, India.
Biometals. 1993 Summer;6(2):133-8. doi: 10.1007/BF00140115.
The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.
通过对大鼠肝脏、肾脏和肠道金属硫蛋白（MT）的诱导、金属的分布以及血液学参数的变化，研究了膳食缺铁对急性镍、铅或镉毒性的影响。镉的给药诱导了肝脏、肾脏和肠道的MT，而镍或铅的给药仅诱导了肝脏MT。然而，膳食缺铁并不影响镉诱导的组织MT，但增强了镍或铅恢复在机体铁状态降低影响下降低的肾脏和肠道MT正常合成的能力。铅在肝脏和肾脏中的蓄积以及镉仅在肝脏中的蓄积增强，而镍的组织沉积不受缺铁的影响。正常大鼠中三种金属对肝脏MT的诱导似乎与肝脏锌、钙和铁水平的同时升高有关。然而，膳食缺铁会使镍或镉作用下的肝脏锌增加，铅作用下的肝脏钙增加。
